id	author	title	date	pages	extension	mime	words	sentence	flesch	summary	cache	txt
dti-1423	Kitanaka, Junichi; Kitanaka, Nobue; Hall, F. Scott; Uhl, George R.; Takemura, Motohiko	Brain Histamine N-Methyltransferase as a Possible Target of Treatment for Methamphetamine Overdose	2016	7	.pdf	application/pdf	5975	484	47	http://www.la-press.com http://www.la-press.com/drug-target-insights-journal-j23 Kitanaka et al 4 Drug TargeT InsIghTs 2016:10 dependently decreased METH-induced stereotypical biting, while increasing sniffing, suggesting that metoprine may ame- liorate high-dose METH-induced symptoms by producing a leftward shift in METH behavioral effects (Table 1).65 In brain, for termination of histaminergic neurotransmission after activa- tion of histamine receptors, histamine is transferred from the extracellular space into cytoplasm by organic cation transporter 3 and/or the equilibrative nucleoside transporter (ENT4), and catabolized by the cytosolic enzyme histamine N-methyltrans- ferase (HMT) to form N-methylhistamine, which is inactive in the histaminergic system.55,56 HMT is the sole enzyme that degrades histamine in brain,57,58 whereas diamine oxidase (DAO; histaminase) catabolizes histamine in peripheral tis- sues.49,59	cache/dti-1423.pdf	txt/dti-1423.txt